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GAESSER, GLENN A.

Abstract

For constant-load, heavy exercise (i.e., above the lactate threshold (TLac.)), a slow component of oxygen uptake ([latin capital V with dot above]O2) is observed. Endurance training reduces the magnitude of the slow component and, hence, end-exercise [latin capital V with dot above]O2. Reductions in exercise [latin capital V with dot above]O2 have been reported after 7-8 wk of training; unpublished observations suggest that the [latin capital V with dot above]O2 slow component may be attenuated after just 2 wk of training. A minimum training intensity for eliciting reductions in constant-load exercise [latin capital V with dot above]O2 has not been established; however, in the elderly, training at an intensity below TLac resulted in similar reductions in exercise [latin capital V with dot above]O2 as did training above TLac. Mechanisms responsible for the reduced slow component of [latin capital V with dot above]O2 after training remain to be firmly established. Evidence both for and against blood lactate concentration ([L-]) as a mediator of the slow component has been published; high correlations between [L-] and the slow component, and between the training-induced reductions in these variables, appear to be more coincidental than causal. Decreased pulmonary ventilation after training may account for between 14% and 30% of the reduction in the slow component of [latin capital V with dot above]O2. Epinephrine infusion does not augment exercise [latin capital V with dot above]O2, nor does [beta]-adrenergic blockade diminish the magnitude of the slow component of [latin capital V with dot above]O2.

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